Abel Viejo-Borbolla is a Junior (W1) Professor in Experimental Virology at the Institute of Virology at Hannover Medical School (MHH). He graduated as a BSc (Hons) in Biological Sciences at the Universidad Autónoma de Madrid (Spain). He coursed the final year of his degree at The University of Leeds (UK) as an Erasmus student. In 2002 he obtained his PhD title from The University of Liverpool (UK) under the supervision of Prof. Thomas F. Schulz (The University of Liverpool) and Dr. Eddie Blair (GlaxoSmithKline, UK). His research focused on improving targeted retroviral vectors for gene therapy and involved the investigation of virus cell entry. From 2002 to 2004 he investigated the pathogenesis of Kaposi’s sarcoma-associated herpesvirus as a postdoc in the laboratory of Prof. Thomas F. Schulz at the Institute of Virology at the MHH. In 2004 he joined the laboratory of Antonio Alcami (first at Centro Nacional de Biotecnología and then at the Centro de Biología Molecular Severo Ochoa, both at Madrid, Spain) where he started his research on immune modulation mediated by herpesviruses. In 2008 he worked as a visiting scientist in the laboratory of Sergio Lira (Mount Sinai School of Medicine, New York, USA) where he generated and characterized several transgenic mouse lines expressing viral immune modulators. Following his return to Madrid in 2009 he led the herpesvirus subgroup under Antonio Alcami’s auspices. In September 2013 he joined the MHH as a Junior Professor.
Research interest and achievements
The main interest of Abel Viejo-Borbolla is to understand how viruses modulate the host at different stages of the viral cycle, from cell entry to viral spread. During his PhD he investigated the route of entry of retrovirus-based vectors used for gene therapy. In the last few years he has focused on the modulation of the immune and nervous systems by the human alphaherpesviruses herpes simplex virus type 1 and 2 (HSV-1 and HSV-2, respectively) and varicella zoster virus (VZV), highly prevalent human pathogens that establish latency in sensory ganglia. He has discovered and characterized several viral chemokine-binding proteins (vCKBP) including the first vCKBP expressed by HSV-1 and HSV-2. Moreover, he has shown that HSV vCKBP, contrary to all previously discovered vCKBP that inhibit chemotaxis, enhances chemokine-mediated migration. Recently, he has participated in the discovery of the ability of HSV-1 and HSV-2 glycoprotein G (gG) to bind neurotrophic factors. Surprisingly, only gG from HSV-2 enhances the activity of nerve growth factor. This constitutes the discovery of the first protein expressed by a pathogen that binds to and modulates neurotrophins. His research opens the door to further studies characterising this interaction and to the investigation of neurotrophin modulation by other relevant human pathogens.